Pathophysiology, Clinical Manifestation and Interventional Management of Ketoacidosis - Case Study Example

Pathophysiology, Clinical Manifestation and Interventional Management of Ketoacidosis (DKA) Patient Name Course/Unit Tutor 12 October 2012 Introduction Mrs. X is aged 49 years. She is admitted at Monash Medical Centre, in the Emergency Department, where she is associated with a 2-day history headache and nausea and vomiting; experienced numerously each day. An assessment is conducted and Mrs. X is found to have an oxygen saturation level of 97% on RA, respiration rate is found to be 24 breaths per minute, heart rate is established to be 132 beats per minute and blood pressure of 89/60 mmHg. At the same time, Mrs. X is found to be alert and orientation with BSL reading of 16mmol/L. Medical history is carried out where it is revealed that Mrs. X suffers from T1DM and exhibits no history of underlying renal or cardiac disease. Further physical examination reveals that Mrs. X has dry and warm skin, poor skin turgor and dry mucous membranes. Besides, diagnosis is carried out and Mrs. X is found to have diabetic ketoacidosis (DKA). As a result, Mrs. X manifests various clinical symptoms: tachycardia, hypotension and polyuria, that are further investigated. Therefore, the essay analyses the three clinical manifestations in terms of their pathophysiology and interventional management strategies. Pathophysiology and clinical manifestations Diabetic ketoacidosis (DKA) is severe and serious condition that comes about as a result of inability of body cells to receive glucose or sugar that is required for energy (Gibbs, 2010). Mrs. X has developed DKA due to total or relative shortage of circulating insulin in the body. At the same time, DKA can be said to have emerged from joint impacts of accelerated levels of counter-regulatory hormones such as catecholamine, glucagon, cortisol, and growth hormone (Steel & Tibby, 2009). Total shortage of insulin has been found to be prevalent among individuals with T1DM (Steel & Tibby, 2009). Moreover, the condition occurs among the patients who while receiving treatment may be tempted to suspend the intake of insulin, especially the long-acting component of a basal-bolus regimen (Wolfsdorf et al., 2007). Lack of insulin or inadequate insulin in Mrs. X’s body is linked to inability of the body to utilise sugar for energy. Furthermore, when the cells find it difficult to receive sugar, the body initiates break down of fat and muscle in order to generate glucose for energy (Gibbs, 2010). When this takes place, the body is able to generate ketones, or fatty acids, which when produced find their way in the bloodstream, causing chemical imbalance, also known as metabolic acidosis, which results in diabetic ketoacidosis (Donahey & Folse, 2012). On the other hand, DKA has been found to develop when inadequate or lack of insulin increases catabolic state that motivates the development of classical picture of DKA with: hyperglycaemia, hyperketonaemia, and hyperosmolality (Jerreat, 2010). Therefore, Mrs. X experiences shortage of insulin that can be said to be responsible for the ketosis and increased glycogenolysis and gluconeogenesis, leading to hyperglycaemia (Jerreat, 2010). Formation of hyperglycaemia increases serum osmolality, which, when combined with reduced insulin, leads to osmotic dieresis (Jerreat, 2010). It is the formation of dieresis that leads to electrolyte abnormalities largely associated with DKA, such as sodium, potassium, calcium, magnesium, chloride, and phosphate abnormalities (Donahey & Folse, 2012). The role of osmotic dieresis is evident in the formation of hypovolemia, which has been found to affect and reduce the perfusion of key organs such as the kidney. Furthermore, when insulin reduces, together with changes in the level of hormones, there is the formation of lipolysis, as well as free release of fatty acids. Besides, the free fatty acids found in the liver are metabolised and transformed into ketones bodies, whereby, high concentration of ketones bodies leads to formation of anion gap metabolic acidosis, which is a prominent characteristic of DKA (Savage, 2011). Tachycardia When an investigation is carried out on Mrs. X, it is established that Mrs. X has a heart rate of 132 beats per minute. At the same time, she experiences headache, nausea, and vomiting, and dehydration. This clearly shows that Mrs. X has Tachycardia (Fowler, 2009).Tachycardia emerge when the heart rate is faster than normal. A healthy grown up individual experiences a heart rate that ranges between 60 to 100 times in every minute; when such an individual is at rest (Fogel & Zimmerman, 2009). Mrs. X has no insulin, or the available insulin in her body is inadequate. This results in the formation of osmotic dieresis, responsible for electrolyte abnormalities, which cause disruption and disorganisation of normal electrical impulses. Eventually, the control of rhythm of the heart’s pumping actions is disrupted, denying other parts of the body oxygen (Fogel & Zimmerman, 2009; Heck, Rosso & Kistler, 2011). At the same time, hypovolemia is also responsible for tachycardia condition. Osmotic dieresis is responsible for the low blood volume in the body of Mrs. X; this is as a result of increase in urination and vomiting (Fowler, 2009). Low volumes of blood in the body results in formation of low quantities of oxygen, a situation that results into diminished effective delivery of oxygen in the body since the level of blood is low. The decreased intake of oxygen, decrease absorption of oxygen, and inadequate transport of oxygen stimulates tissues for abnormal demand of oxygen increase. Therefore, Mrs. X experiences increased heart pumping actions in an attempt to increase the level of oxygen (Fowler, 2009). As this happens, the heart impulses increase and become rapid, which later affects proper pumping of the blood to the heart and in the rest parts of the body. The event further suffocates the circulation of oxygen available, hence, leading to tachycardia. Hypotension When Mrs. X is admitted to the hospital, investigations reveals that she is experiencing nausea and her blood pressure is 89/60mmHg. The two signs clearly show that Mrs. X suffers from hypotension. In normal cases when Mrs. X sits up or stand, the blood flow in her body should be able to move to her legs and away from her heart and brains (Karl, 2010). When this takes place, the legs muscles squeeze blood back to the heart and the heart is able to increase the rate of blood pump to the brain (Karl, 2010). This normal process is disrupted in the case of Mrs. X given her situation where she suffers from T1DM. Mrs. X develops a condition known as hypotension. In most cases, individuals found to have blood pressure of 90/60 mmHg or lower, are regarded to have hypotension (Karl, 2010). The electrolyte abnormalities disorganise the normal electrical impulses in the body (Fagan, Avner & Khine, 2008). In this case, electrolyte abnormality in the case of Mrs. X is responsible for disruption and disorganisation of compensatory neuronal, humoral and endotheliah mechanisms that influence adaptability of heart rate (HR), stroke volume, cardiac contractility, vascular resistance and venous capacitance (Kisiel & Marsons, 2009). As a result, when the patient stands up after a period of recumbence, there is disruption in the normal displacement of 300-1000ml of blood into the veins of the legs, pelvis and abdomen (Daugirdas, Blake & Ing, 2006). Besides, this displacement is unusual slow affecting the redistribution that takes place in the pelvic and upper leg veins. In the normal case, blood pressure when an individual attain upright posture should facilitates reduction in venous return to the heart by 25-30%, which should lead to a transient reduction in stroke volume of about 40% (Karl, 2010). In the case of Mrs. X, the cardiac output is affected and this leads to inadequate acute compensatory increase in HR, systematic vascular resistance and venous tone that later result in creation of imbalance in the maintenance of tissue perfusion, hence, emergence of hypotension. Polyuria Further investigation of Mrs. X reveals the presence of T1DM. She demonstrates to have dry and warm skin, poor skin turgor and dry mucous membranes. DKA results in formation of hyperglycaemia that facilitates an increase in serum osmolality (Graczyk et al., 2011), which, when combined with reduced level of insulin, leads to osmotic dieresis. It is the formation of osmotic dieresis that leads to formation of an electrolyte abnormality that facilitates excessive production of urine (Graczyk et al., 2011). The role of osmotic dieresis is further noted in the formation of hypovolemia, which has been found to affect and reduce the perfusion of key organs such as the kidney. The primary unit in the kidney that participates in this function is the nephron that is composed of a glomerulus, proximal tubule, loop of Henle, distal tubule, and collecting duct (Grauer, 2004). Urine formation takes place in each nephron and three primary processes are involved glomerular filtration, tubular re-absorption, and tubular secretion. The walls of glomerular capillaries are porous to water and small-molecular-weight molecules that include electrolytes, glucose and amino acids. At the same time, blood cells and most plasma proteins are retained in the glomerular capillary lumen and leave the glomerular capillaries through the efferent arteriole (Grauer, 2004). Re-absorption of substances such as sodium, glucose, and amino acids, in the tubular result in tubular secretion of organic ions, potassium, and protons that determine the composition of urine (Karl, 2010). In the case of Mrs. X, the absorption of about 75% of filtered water has to occur passively in the proximal tubule along the osmotic gradients that is established by active transport of solutes such as sodium, potassium, bicarbonate, amino acids, and glucose. Obligatory water re-absorption should occur in the proximal tubule regardless of the body’s actual need for water. The formation of hyperglycaemia facilitates increase in serum osmolality and osmotic dieresis causes electrolyte abnormality in the kidney and to extent the proximal tubule (Natsume, 2007). As a result, impairment occurs in the proximal tubule that makes it impossible for re-absorption of water to take place. Furthermore, abnormal concentration of sodium, potassium, calcium, magnesium, chloride, and phosphate lead to impairment of the renin-angiotensin system that facilitates excessive production of urine. Management and intervention The primary goals in treatment of DKA are to provide adequate insulin in proper quantity, conduct rehydration of the patient, and ensuring appropriate potassium level is maintained (Crocetti & Barone, 2004). Besides, quality care management is essential in the whole process of treatment and management of DKA. Fluid replacement Fluid replacement in the case of Mrs. X is largely aimed at reducing the impact of dehydration. When Mrs. X is admitted at Monash Medical Centre, she is investigated and found to be experiencing nausea and also vomiting. This actually shows that Mrs. X has lost some water in the body that explains her dehydration situation. At the same time, water loss is due to polyuria condition that is caused by osmotic dieresis, which later leads to vomiting. Further indications of dehydration are manifested by symptoms such as dry mucous membrane, poor skin turgor and hypotension condition (Crocetti & Barone, 2004). The fluid replacement process for Mrs. X begins immediately she is diagnosed. An isotonic solution, saline (NS), is used in this case given its ability to help restore the intravascular volume, thereby, maintain blood pressure and kidney perfusion (Karen et al., 2008). This process enhances glucose loss through the kidney resulting in a lower blood glucose level. In the first hour of fluid replacement, Mrs. X is given 20mL/kg of NS and this is followed by assessment of Mrs. X state of hydration in the next hour to see the reaction of this process (Razavi & Amanati, 2011). In the second hour, another 20mL/kg of NS is again administered as the patient is monitored. In the subsequent hours, the rate of NS is reduced slightly to 15mL/kg as the patient shows progressive positive signs of reaction. The increase in NS administration is to ensure proper perfusion is realised in Mrs. X. The initial goal in this first phase is to rectify the intravascular volume through administration of isotonic saline. After the accomplishment of this process, Mrs. X is later administered with hypotonic saline (0.45 NS) in the next 24 to 48 hours to correct acidosis. Appropriate measures are observed throughout the process to ensure that no excess fluid replacement is carried out in order to avoid symptomatic brain swelling and pulmonary oedema (Razavi & Amanati, 2011). Potassium replacement Potassium in most cases is absent in patients diagnosed with DKA, although measured serum potassium may be high, normal or low due to inter-current acidosis (Pescovitz & Eugster, 2004). Osmotic dieresis causes large loss of potassium, and other minerals. Therefore, potassium replacement is necessary in the case of Mrs. X. Careful management has to be observed in potassium management in order to avoid emergence of hypokalaemia and hyperkalaemia, since these two can occur during the process of treatment, and they are dangerous to the life of the patient (Pescovitz & Eugster, 2004). Potassium replacement aims to restore the glomerular filtration rate in order to allow for increased urinary potassium losses. The initial replacement should start with administration of normal saline, before determining the serum potassium level to administer (Koul, 2009). Before the process of potassium replacement is administered to Mrs. X, a test is carried out to establish the initial concentration of serum and also the resilience of renal output of the patient. The above activities takes place in the first hour of treatment or immediately the patient is received in the medical centre. In the second hour of treatment the process to infuse Mrs. X with potassium is established, whereby, potassium is administered at the rate of 10 to 20 mmol per every hour in the first two hours (Pescovitz & Eugster, 2004). In the next three hours, quantity of potassium is slightly reduced in accordance to observations that are made in the process of monitoring the serum potassium concentration. In the case of Mrs. X, it is established that her serum potassium is between 3 to 4 mmol/L; hence the patient is infused with 30mmol per every hour in the next three hours (Pescovitz & Eugster, 2004). This rate is regarded to be safe for the patient. Continuous monitoring and management of patient reaction remains critical in the entire process of treating Mrs. X. Insulin replacement It has been established that rehydration alone is responsible for the improvement of tissue perfusion and renal function; responsible for improving clearance of glucose and ketones (Kearney & Dang, 2007). In this way, insulin is necessary to suppress lipolysis and ketogenesis in Mrs. X (Kitabchi, Murphy, Spencer, Matteri & Karas, 2008). At the same time, the production of ketones in Mrs. X has to stop, hence the need for insulin replacement. Furthermore, the metabolism of the patient has to be enhanced. As a result, administration of insulin will enable Mrs. X to realise enhanced production of bicarbonate (HCO3) and improvement of academia. In most cases, patients with DKA are advised to have continuous administration of intravenous insulin, which is regarded as a form of standard care. Insulin replacement in the case of Mrs. X is carried out using short-acting insulin, and the intravenous route is chosen as the preferred method (Karen et al., 2008). The advantage associated with a continuous intravenous insulin infusion is the elimination of the problem of poor absorption from subcutaneous and intramuscular sites, especially in a dehydrated patient like Mrs. X (Karen et al., 2008). Another advantage has to do with rapid clearance that allows easy dose adjustment, and this makes management more controllable. The process starts by infusion of 0.1 units/kg/hour. At the same time, a bolus of the same dose is administered before the insulin infusion is carried out. Besides, the infuscate is run between 30-50mL, through the tubing to saturate binding sites on the tubing. Furthermore, insulin infusion is given separately from the replacement fluids and this makes the rates easy to adjust independently (Koul, 2009). Moreover, in infusion pump is used throughout the process. Throughout the process, the intramuscular route of insulin delivery is used, which proves to be successful, thereby, giving 8 to 10 units of insulin every hour. Glucose therapy Administration of glucose decreases in each hour at a rate of about 75 to 100mg/dL/ hour (Crocetti & Barone, 2004). During the first hour of treatment, a decrease in glucose level is realised from the initial rehydration fluids, which occurs as intravascular volume expands. The blood glucose level corrects to normal level more quickly than the acidosis does, and this calls for continuation of intravenous insulin until the acidosis is cleared. In the case of Mrs. X, the glucose level in the blood is determined and acidosis found to be present. Glucose is therefore added to the intravenous fluids starting with 5% dextrose. This is increased as the need arise to 7.5% dextrose in order to keep the blood glucose at about 250mg/Dl. Initially, it is established that Mrs. X blood glucose level is less than 300, and this makes it necessary to add 5% dextrose at the onset of the treatment (Crocetti & Barone, 2004). The process continues gradually with great level of monitoring and care management. Other management Treating DKA is the first profound step for Mrs. X, thereafter, there is need to initiate an after-care management plan and process for the patient. After the acute episode of DKA has been resolved effectively, Mrs. X needs appropriate training and education that incorporate continuous communication between the Mrs. X and the medical practitioner (Devalia, 2010). This is important and necessary to ensure that future prospects for the condition recurring are minimised since Mrs. X is empowered to identify, prevent and manage symptoms associated with DKA when detected early. At the same time, education is necessary to ensure effective future prevention process and strategies are successful. Key areas that Mrs. X should be trained and educated in are sick day management, blood glucose targets and detection, ketones testing, and education of other family members in order to ensure they are effectively incorporated in the care programme and process (Southern Health, 2012). On the other hand, Mrs. X has to be monitored frequently and on continuous basis after the discharge. This is particularly important to ensure that appropriate steps and actions are followed in ensuring that Mrs. X acquires appropriate diabetes education, assessment of nutrition is thoroughly carried out, physical and psychological assessment is conducted, and referral to diabetes support groups and services is enhanced or initiated (Southern Health, 2012). All these activities ensure that Mrs. X receives a holistic and quality recovery process that gives her a chance to live fruitful live again. Conclusion The case study has successfully looked at Mrs. X’s clinical manifestations of hypotension, polyuria and tachycardia that explain the patient’s medical condition of diabetic ketoacidosis (DKA). Other relevant symptoms identified are dry and warm skin, poor skin turgor and dry mucous membranes that further explain that Mrs. X is suffering from DKA. Pathophysiology of these clinical manifestations is carried out where management interventions deemed to be appropriate for Mrs. X, include fluid replacement, potassium replacement, insulin replacement, and glucose therapy. At the same time, it is established that other management in terms of after-care management planning and management is necessary to ensure Mrs. X experience a holistic recovery process. Examples of these management strategies include appropriate training and education that incorporate continuous communication, education to ensure effective future prevention process and strategies are successful, and day care management programme that incorporate blood glucose targets and detection, ketones testing, and education of other family members. References Crocetti, M., & Barone, M. A. (2004). Oski's Essential Pediatrics. Philadelphia: Lippincott Williams & Wilkins. Daugirdas, J. T., Blake, P. G., & Ing, T. S. (2006). Handbook of Dialysis. 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